Medicine Bi-monthly Assessment (May)

 

31/5/2021
Samhita Ghanathay

I have been given the following cases in an attempt to understand the topic of "Patient Clinical Data Analysis", to develop my competency in reading and comprehending clinical data- including history, clinical findings, investigations and diagnosis - and  come up with a treatment plan.

Following is the link to the set of questions given to me -

http://medicinedepartment.blogspot.com/2021/05/online-blended-bimonthly-assignment.html?m=1

Below are my answers to Medicine Assignment based on my comprehension of the case.

PULMONOLOGY:

CASE A: Exacerbation of COPD

Link to the case:

https://soumyanadella128eloggm.blogspot.com/2021/05/a-55-year-old-female-with-shortness-of.html

Question 1:

What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

Evolution of symptomatology:

Ø  20 years ago – 1^st episode of shortness of breath

Ø  Next  8 years – similar episodes 1/year ,lasting a week

Ø  12 years ago – a more severe episode of shortness of breath – hospitalized

Ø  Next 12 years  - similar episodes 1/year

Ø  8 years ago – diagnosed with diabetes

Ø  5 years ago – diagnosed with anemia

Ø  1 month ago – generalized weakness

Ø  20-days ago - diagnosed with hypertension

Ø  15-days ago -  pedal edema and facial puffiness

Anatomical localization :

LUNGS (bronchi and bronchioles) – lesions here led to increased pulmonary blood pressure thus causing Right Heart Failure.

Primary Etiology :

• This condition is seen to reoccur every year around the same time and area of work, thus suggesting that it is an allergic reaction to Paddy dust.
• Apart from that there is a history of use of CHULHA for years – which might have aggrevated the condition in following years.

Question 2:

What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?

Pharmacological interventions:

	MOA	INDICATIONS	EFFICACY
Inj. Augmentin	Beta-lactum antimicrobial – inhibits peptidoglycan layer formation.
Tab.Azithromycin	Inhinits bacterial protein synthesis
Inj.Lasix	Loop diuretic	Pulmonary HTN
Tab.Pantop	Inhibits final step in Gastric acid production	Compensated respiratory acidosis?
Inj.Hydrocortisone	Decrease leukocyte migration to injured area	Inflammation  in the area of lesion
Neb with ipravent, budecort	Bronchodilator and anti-inflammatory	SOB
Tab. Pulmoclear	Loosens mucosa	SOB
Inj.HAI	Fast acting insulin	Diabetes
Inj.Thiamine	-	Vitamin B1 deficiency

 

Non-pharmacological interventions:

·         Head elevation : Increases end expiratory lung volume and improves oxygenation.

·         O2 inhalation : To manage hypoxia and Increase oxyHb in RBC

·         BiPAP intermittent : To relieve overworked lung and chest wall muscles (provides custom air pressure for inhalation and exhalation)

·         Chest physiotherapy: To improve Respiratory efficiency and lung capacities by strengthening of chest wall muscles

·         Vitals charting : For a constant check on patient

·         Urine Input/Output charting (I/O) -  used to assess water/fluid dynamics in the body, depending upon fluid intake, urine volume and output over 24 hours.

Question 3:

What could be the causes for her current acute exacerbation?

·         No data available for diagnosis of TB. Assuming it was a provisional diagnosis, even the adviced medication  is not mentioned in the case sheet. Events related to this medication could have led to the exacerbation of COPD. (detailed in the next bit).

·         Environmental pollutants 

Question 4:

Could the ATT have affected her symptoms? If so how?

• Yes.
• Drugs used in 1^st line treatment of TB namely Izoniazid and Rifampicin are known to be nephrotoxic in nature.
• The damaged kidneys may have led to cardiorenal syndrome which inturn effected the lung and affected her symptoms.

Question 5:

What could be the causes for her electrolyte imbalance?

Possible causes are

Hyponatrimia :

• Right heart failure
• Respiratory acidosis
• Worsening hypoxia

Hypochloremia : Compensated respiratory acidosis .

NEUROLOGY:

CASE A : Altered sensorium

Link to the case:

https://143vibhahegde.blogspot.com/2021/05/wernickes-encephalopathy.html

Question 1: 

What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

Evolution of symptomatology :

1 year ago – 1^st episode of seizures

4 months ago – latest episode of seizures

                          Alcohol withdrawal symptoms : restlessness, sweating, tremors (following      which he started drinking again)

09/5/2021 – Laughing and talking to self

                    Oriented only from time to time

                    Could not lift himself from bed

                    Difficulty in walking without support

                    Developed short term memory loss

                    (stopped drinking alcohol)

15/5/2021 – Admitted to the hospital

 Anatomical localization : Hippocampus.

Primary etiology : Vitamin B1 stores in body exhausted – biochemical lesions formed in the brain – thus the symptoms. 

Question 2:

What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?

	MOA	INDICATIONS	EFFICACY
IVF NS	Electrolyte replacement	Dehydration (due to excessive alcohol)
Inj.THIAMINE	-	Vitamin B1 deficiency
Inj. Lorazepam	Benzodiapene – GABA agonist	Anxiety and sleeplessness
T. Pregabalin	Inhibitory action on neuronal excitation	Anxiety
Inj. HAI	Fast acting insulin	Diabetic control
Lactulose	Reduces levels of ammonia in blood	To improve mental status
Inj KCl	-	Hypokalemia
GRBS 6th hourly	-	K/C/O DM2
Syp Potchlor	-	Hypokalemia

 

Question 3:

 Why have neurological symptoms appeared this time, that were absent during withdrawal earlier? What could be a possible cause for this?

This happens due to KINDLING - refers to the phenomenon of increasingly severe withdrawal symptoms, including an increased risk of seizures, that occurs as a result of repeated withdrawal from alcohol or other sedative–hypnotics with related modes of action.

Alcohol abuse with repeated withdrawal episodes lead to altered brain functions such as:

• Imbalance of inhibitory/excitatory neurotransmitters
• Neuroendocrine dysregulation

This leads to various consequences like:

• Increased seizure susceptibility
• Increased anxiety
• Increased neurotoxicity
• Altered persecptions

All this ultimately lead to drinking relapse.

Question 4:

 What is the reason for giving thiamine in this patient?

• Excessive alcohol intake over prolonged periods cause deficiency of Vitamin B1(Thiamine) in the body.
• It is needed for conduction of nerve signals – deficiency of the  same leads to confusion and ataxia – both are seen in this patient.
• Thus Thiamine has been prescribed.

Question 5:

What is the probable reason for kidney injury in this patient?

•   High levels of urea suggest an acute condition.
•   High serum creatinine points to a prerenal condition – suggesting the reason for kidney failure      to be dehydration (AKI ultimately leading to Acute tubular necrosis).

Question 6:

 What is the probable cause for the normocytic anemia?

Reason for normocytic anemia:

• Chronic alcoholism causes iron deficiency leading to reduced hemoglobin in blood and thus anemia.
• Kidney disease of the patient results in reduced erythropoietin release into blood causing reduced RBC production and anemia.
• The constant bleeding from ulcer may also contribute.

Question 7:

Could chronic alcoholism have aggravated the foot ulcer formation? If yes, how and why?

Yes. Chronic alcoholism is known to cause Peripheral neuropathy -  which along with existing condition of diabetic neuropathy may lead to formation of Non-healing ulcer on foot.

CASE B : Cerebellar Ataxia

Link to the case:

https://kausalyavarma.blogspot.com/2021/05/a-52-year-old-male-with-cerebellar.html?m=1

Question 1:

What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

Evolution of symptomatology :
13/5/2021 – Giddiness and vomiting (1 epidsode)
15/5/2021 – Giddiness (increased)
                     Bilateral hearing loss, aural fullness, tinnitus
                     Vomiting
                     Postural instability

Anatomical localization : right inferior cerebellar hemisphere

Primary etiology : high cholesterol levels  -> embolization -> infarct -> ataxia

Question 2:
What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?

	MOA	INDICATIONS	EFFICACY
Tab Veratin	Histamine analogue	Vertigo; Tinnitus
Inj Zofer	Serotonin inhibitors	Gastric problems
Tab Ecosprin	Inhibits formation of thromboxane A2	Presence of blood clot(infarct)
Tab Atorvostatin	Inhibits HMG-COA reductase	High cholesterol
Tab Clopidogrel	Inhibits ADP mediated glycoprotein activation	-
Inj Thiamine	-	Vitamin B1 deficiency
Tab MVT	-	Vitamin b12 deficiency
BP Monitoring	-	-

 

Question 3:
Did the patients history of denovo HTN contribute to his current condition?

NO. (other way round is possible).

 

Question 4:
Does the patients history of alcoholism make him more susceptible to ischaemic or haemorrhagic type of stroke?

 Yes – hemorrhagic type –liver 

CASE C: Cervical spondylosis and recurrent hypokalemic paralysis.

Link to the case:

http://bejugamomnivasguptha.blogspot.com/2021/05/a-45-years-old-female-patient-with.html

Question 1:

What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

Evolution of symptomatology:
August 2019 – Bipedal edema (pitting type)
12/5/2021 – pain in left arm
13/5/2021 – Chest pain
13/5/2021 – Difficulty in breathing (NYHA-CLASS-3)
13/5/2021 – Palpitations (more at night, increased since last night)

Anatomical localization: vertebral discs between C2, C3 and C4 vertebral bodies

Primary etiology :  Spondylosis : aging
                          Hypokalemia : genetic

Question 2:

What are the reasons for recurrence of hypokalemia in her? Important risk factors for her hypokalemia?

 Hypokalemic periodic paralysis – a genetic disorder is a possible reason for recurrence of the hypokalemia.

Question 3:

What are the changes seen in ECG in case of hypokalemia and associated symptoms?

• Flattening and inversion of t-wave. QT interval prolongation and St depression in severe cases.
• Associated symptoms: weakness, fatigue, muscle cramps, worsening of diabetes, palpitations.

CASE D: Seizures.

Link to the case:

https://rishikoundinya.blogspot.com/2021/05/55years-old-patient-with-seizures.html

Question 1:

Is there any relationship between occurrence of seizure to brain stroke. If yes what is the mechanism behind it?

Yes  (patient has most likely suffered ischemic stroke)

Seizure is defined as sudden alteration of behavior due to a temporary change in the electrical functioning of the brain.

Stroke is defined as damage to the brain from interruption of its blood supply.

Mechanism :

A stroke - brain is injured

↓

Scar tissue formed in area of injury

↓

Affects the electrical activity in brain

↓

Disrupting the electrical activity

↓

Seizure.

Question 2:

In the previous episodes of seizures, patient didn't loose his consciousness but in the recent episode he lost his consciousness what might be the reason?

There is a possibility that over time the infarct grew in size, causing increased pressure over surrounding area, leading to unconsciousness in the latest episode of seizure.

CASE E: Seizures ans altered sensorium.

Link to the case:

https://nikhilasampathkumar.blogspot.com/2021/05/a-48-year-old-male-with-seizures-and.html?m=1

Question 1:

What could have been the reason for this patient to develop ataxia in the past 1 year?

Possibly an untreated and thus an unregistered fall leading to head injury a year ago, led to intracranial hemorrhage – causing pressure on brain areas and ataxia.

Question 2:

What was the reason for his IC bleed?Does Alcoholism contribute to bleeding diatheses?

• In the new study, drinking alcohol causes liver damage  - leading to decreased clumping  of clotting cells in the blood.  
• The impaired platelet function, together with the reduced platelet count, may contribute to the bleeding diathesis associated with chronic alcoholism.
• Considering the episode of binge drinking approximately 3 hours ago, the excessive amout of metabolized alcohol might have led to IC bleed followed by seizures.

CASE F: Right sided CVA.

Link to the case:

http://shivanireddymedicalcasediscussion.blogspot.com/2021/05/a-30-yr-old-male-patient-with-weakness.html

Question 1:
Does the patient's  history of road traffic accident have any role in his present condition?

Yes, there may be an association between the two events.
An unidentified injury at that time might have developed over 4 years into a clot now leading to infarct.

Question 2:
What are warning signs of CVA?

Warning signs of CVA include :
• Sudden onset of weakness or numbness on one side of the body.
• Sudden speech difficulty or confusion.
• Sudden difficulty seeing in one or both eyes.
• Sudden onset of dizziness, trouble walking or loss of balance.
• Sudden, severe headache with no known cause
 

Question 3:
What is the drug rationale in CVA?

• Mannitol : The role of mannitol therapy in acute stroke is controversial. Because of its osmotic effect, mannitol is assumed to decrease cerebral edema. Mannitol might improve cerebral perfusion by decreasing viscosity, and as a free-radical scavenger, it might act as a neuroprotectant.

• Ecosprin-Aspirin(antiplatelet drug) : Aspirin irreversibly inhibits cyclooxygenase, which prevents the conversion of arachidonic acid to thromboxane A2 (TXA2). Thromboxane A2 is a vasoconstrictor and stimulator of platelet aggregration. Platelets are inhibited for their full life cycle (5–7 days) after exposure to aspirin. Aspirin also inhibits prostacyclin activity and this inhibits platelet aggregration. The effects of aspirin on prostacyclin are dose related.

• Atorvastatin belongs to a group of medicines called statins. It's used to lower cholesterol if you've been diagnosed with high blood cholesterol. It's also taken to prevent heart disease, including heart attacks and strokes.

 
Question 4:
 Does alcohol has any role in his attack?

 I would like to highlight 2 points here:

• Normally, excessive alcohol ( most studies define excessive as more than 2 glasses each day) may lead to liver dysfunction. This causes reduced production of substances that aid in blood clotting, increasing the risk of stroke.
• On the other hand, over a long period of time, alcohol consumption may lead to increased risk of hypertension wich inturn is a risk for infarct typr of stroke.

Considering he is an occasional drinker and has no history of hypertension, in this case the role of alcohol in stroke seems insignificant.

 

Question 5:
Does his lipid profile has any role for his attack??

 Yes it is does have a role.
Patient’s lipid profile shows low levels of HDL and normal levels of LDL – thus suggesting increased cholesterol levels in the body, associating with increased risk of plaque formation in the vessels.

Increased cholesterol levels

↓

Increased risk of plaque formation

↓

Possible embolization

↓

Infarct.

CASE G:Cervical myelopathy.

Link to the case:

https://amishajaiswal03eloggm.blogspot.com/2021/05/a-50-year-old-patient-with-cervical.html

Note: Cervical Mylopathy – a degenerative condition caused due to pressure on spinal cord. It is characterized by clumsiness in hands and gait imbalance.

Question 1:
What is myelopathy hand ?

• It ia condition associated with Cervical Mylopathy .
• In this - There is loss of power of adduction and extension of the ulnar two or three fingers and an inability to grip and release rapidly with these fingers. It appear to be due to pyramidal tract involvement.
• Treatment is surgical – with improved power, but no permanent cure.

Question 2:
What is finger escape ?

• It is also seen in Cervical Mylopathy. Also known as Wartenberg's sign
• It is a neurological sign that is characterized by involuntary abduction of the 5^th finger/little finger – caused by unopposed aqction of extensor digiti minimi.
• The correction is surgical -  using a slip of the extensor digitorum communis of the ring finger.

Question 3:
What is Hoffman’s reflex?

• It is a test that doctors use to examine the reflexes of the upper extremities.
• This test is a quick, equipment-free way to test for the possible existence of spinal cord compression from a lesion on the spinal cord or another underlying nerve condition.

Procedure: The Hoffmann's reflex test itself involves loosely holding the middle finger and flicking the fingernail downward, allowing the middle finger to flick upward reflexively. A positive response is seen when there is flexion and adduction of the thumb on the same hand.

Interpretations

• A positive Hoffmann’s reflex and finger jerks suggest -  hypertonia, but can occur in healthy individuals, and are not useful signs in isolation. In cerebellar diseases, the reflexes may be pendular, and muscle contraction and relaxation tend to be slow, but these are not sensitive or specific to cerebellar signs
• Absent Hoffman’s  reflexes are characteristic of acute inflammatory demyelinating polyneuropathy (Guillain–Barré syndrome). This loss of H reflexes occurs early and may be an isolated finding in patients studied within several days after onset of illness

CASE H:.Seizures

Link to the case:

https://neerajareddysingur.blogspot.com/2021/05/general-medicine-case-discussion.html?m=1    

Cerebral venous sinus thrombosis (CVST) occurs when a blood clot forms in the brain’s venous sinuses. This  prevents blood from draining out of the brain. As a result, blood cells may break and leak blood into the brain tissues, forming a hemorrhage.

This chain of events is part of a stroke that can occur in adults and children. It can occur even in newborns and babies in the womb. A stroke can damage the brain and central nervous system. A stroke is serious and requires immediate medical attention.
This condition may also be called cerebral sinovenous thrombosis.
 

Question 1:
What can be  the cause of her condition ? 

The causes of seizures in this patient can be

•Electrolyte imbalance(hypomagnesimia)

•Iron deficiency anemia(mainly in endemic area of malaria)

•hypogylcemia 

 

Question2:
What are the risk factors for cortical vein thrombosis?

Also known as superficial cerebral vein infarct, its risk factors in general include :

• Excessive blood clot formation.
• Sickle cell anemia.
• Chronic hemolytic anemia.
• Beta-thalassemia major.
• Heart disease — either congenital (you're born with it) or acquired (you develop it)
• Iron deficiency.
• Dehydration

 
In addition, the risk factors for adults include :

• Pregnancy and the first few weeks after delivery
• Problems with blood clotting- for example, antiphospholipid syndrome
• Cancer
• Collagen vascular diseases like lupus, Wegener’s granulomatosis, and Behcet syndrome
• Obesity
• Low blood pressure in the brain (intracranial hypotension)
• Inflammatory bowel disease like Crohn’s disease or ulcerative colitis

 
Question 3 :
There was seizure free period in between but again sudden episode of GTCS why?resolved spontaneously  why?   

Normally, When the disturbed neuronal signals stops, the person's condition is reversed to normal.
 
 
Question 4:
What drug was used in suspicion of cortical venous sinus thrombosis?

 Acitrom tablet is an oral anticoagulant medicine that is used for the treatment and prevention of the formation of abnormal blood clots (thrombus) in blood vessels and disease associated with it affect.

CARDIOLOGY:

CASE A: Acute pericarditis 

Link to the case:

https://muskaangoyal.blogspot.com/2021/05/a-78year-old-male-with-shortness-of.html.

Question 1 :
What is the difference btw heart failure with preserved ejection fraction and with reduced ejection fraction?

• Preserved ejection fraction (HFpEF) – also referred to as diastolic heart failure. The heart muscle contracts normally but the ventricles do not relax as they should during ventricular filling (or when the ventricles relax).
• Reduced ejection fraction (HFrEF) – also referred to as systolic heart failure. The heart muscle does not contract effectively, and therefore less oxygen-rich blood is pumped out to the body.

 

Question 2 :
Why haven't we done pericardiocenetis in this pateint? 

The above case is that of Pericardial effusion.
PERICARDIOCENTESIS is indicated in the following cases-

• Cardiac tamponade
• Large or symptomatic  pericardial effusion 
• Highly suspected TB
• Purulent or neoplastic etiology.

 Since patient is responding to the given medication, we have opted against pericardiocentesis to avoid the possible complications seen after the procedure.

 
Question 3:
What are the risk factors for development of heart failure in the patient?

Risk Factors for development of HF are:

• Hypertension
• Diabetes
• Smoking
• Alcoholic

 
Question 4:
What could be the cause for hypotension in this patient?

Cardiac tamponadeis a complication of pericarditis - happens if too much fluid collects in the sac, putting pressure on the heart. This prevents the heart from properly filling with blood, so less blood leaves the heart, causing a sharp drop in blood pressure

CASE B: Heart Failure 

Link to the case:

https://muskaangoyal.blogspot.com/2021/05/a-73-year-old-male-patient-with-pedal.html. 

Question 1:

What are the possible causes for heart failure in this patient?

? GFR

Calcification of aorta could have extended to the mitral valve. This resulted in left ventricular hypertrophy , causing reduced ejection ratio and thus the congestive heart failure.

Question 2:

What is the reason for anaemia in this case?

• It has been mentioned that the patient has CKD.
• Normally, Kidney produces erythropoietin that is needed for RBC production. In a CKD case, there might be reduced production of this hormone leading to anemia.

Question 3:

.What is the reason for blebs and non healing ulcer in the legs of this patient?

• Heart failure leading to reduced perfusion could be a cause of slow healing.
• Anemia results in reduced nutritional supply contributes to the same.
• Uncontrolled diabetes could be countributing to slow healing.

Question 4:

What sequence of stages of diabetes has been noted in this patient?

 There are four  stages of type 2 DM known :

• Insulin resistence
• Prediabetic
• Diabetic
• Diabetic with vascular complications

Because the patient is suffering from Diabetic Retinopathy, he is at the stage 4 of sequence of stages of  Diabetes.

CASE C: A-Fib and Biatrial thrombus

Link to the case:

https://preityarlagadda.blogspot.com/2021/05/biatrial-thrombus-in-52yr-old-male.html

Question 1:
What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

Evolusion of symptomatology:

10 years ago - inguinal hernia surgery

3 years ago - on and off pain at surgical site and facial puffiness

1 year ago - SOB and Hypertension

2 days ago - Decreased urine output ans SOB
 
Anatomical localization : blood supply to SA Node region has to be verified by examining the coronary vessels relating to that area.
 
Primary etiology :

• SOB if caused by an obstructive lung disease, could lead to increased pressure on heart and if undiagnosed for a long time may lead to A-fib
• H/o hypertension
• Alcoholic

Question 2:
What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?

	MOA	INDICATIONS	EFFICACY
Inj.Dobutamaine	Ionotropic action Weak conotropic action	A-Fib CCF
Tab.Digoxin	Ionotropic action	A-Fib CCF
Inj.Unfractionated Heparin	Inactivates thrombin and activated factor 10A	Atrial thrombus
Tab,Carvediol	Beta blocker	A-Fib
Tab.Acetyl cystine	Mucolytic	-
Tab. Acitron	anticoagulant	Atrail thrombus
Tab.Dytor	Loop diuretic	Cardiorenal syndrome
Tab.Pan D	PPI	Gastric irritation
Tab.Taxim	Antibiotic	Infection
Inj.Thiamine	-	Vitamin B1 deficiency
Inj.HAI	Fast acting insulin	Diabetes

Question 3:
What is the pathogenesis of renal involvement due to heart failure (cardio renal syndrome)? Which type of cardio renal syndrome is this patient? 

                                                                       Kidney failure

                                                                                   ↓

Reduced renal blood flow

↓

Reduced GFR

↓

Increased extracellular fluid volume

↓

Increased pressure on heart( which over a period of time may lead to a-fib).

This case is an example of stage 4 of Cardiorenal syndrome.

Note:
Cardiorenal syndrome type 4 (CRS type 4) is characterized by primary chronic kidney disease (CKD) leading to an impairment of cardiac function, with ventricular hypertrophy, diastolic dysfunction, and/or increased risk of adverse cardiovascular events. 

 

Question 4:
What are the risk factors for atherosclerosis in this patient?

Lipid profile not available to comment on atherosclerosis.

The general reasons for atherosclerosis are as follows:

• High blood pressure
• High cholesterol
• High triglycerides
• Hypertension
• Diabetes and insulin resistance
• Smoking

Question 5:
Why was the patient asked to get those APTT, INR tests for review?

• To examine and evaluate the clotting risk(leading to CAD) in the patient
• If there is a plan for the surgery.

CASE D:Acute Coronary Syndrome 

Link to the case:

https://daddalavineeshachowdary.blogspot.com/2021/05/67-year-old-patient-with-acute-coronary.html?m=1

Question 1:
What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

Evolution of symptomatology :
Since 1 year – Heartburn like episodes
13/5/2021 – Sweating on excertion
                       Shortness of breath at rest
14/5/2021 – Shortness of breath 30 minutes before coming to the hospital
 
Anatomical location : Heart
 
Primary etiology :

• K/C/O Diabetes mellitus – type 2 since 1 year
• K/C/O Hypertension since 6 months

 The above r risk factors that have contributed to current state of the patient.
 

Question 2:
What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?

	MOA	INDICATIONS	EFFICACY
Tab. Metaprolol	Beta blocker	High blood pressure. NSTEMI
PCI	Surgical technique to treat Coronary artery blocks	Non–ST-elevation acute coronary syndrome (NSTE-ACS)   Angina .

 

Question 3:
What are the indications and contraindications for PCI?

Indications:

• Acute ST-elevation myocardial infarction (STEMI)
• Non–ST-elevation acute coronary syndrome (NSTE-ACS)
• Unstable angina.
• Stable angina.
• Anginal equivalent (eg, dyspnea, arrhythmia, or dizziness or syncope)
• High risk stress test findings.        

Contraindications:

• Intolerance for oral antiplatelets long-term
• Absence of cardiac surgery backup.
• Hypercoagulable state.
• High-grade chronic kidney disease
• Chronic total occlusion of SVG
• An artery with a diameter of <1.5 mm.

 
Question 4:
What happens if a PCI is performed in a patient who does not need it? What are the harms of overtreatment and why is research on overtesting and overtreatment important to current healthcare systems?

There is no harm done apart from the general complications of PCI like :

• Injury to the heart arteries, including tears or rupture
• Infection, bleeding, or bruising at the catheter site
• Allergic reaction to the dye or contrast used
• Kidney damage from the dye or contrast
• Blood clots that can lead to stroke or heart attack
• Bleeding into the abdomen (retroperitoneal bleeding).

HARMS OF OVERTREATMENT AND OVERDIAGNOSIS:

• psychosocial stressors
• renal morbidity
• unnecessary surgical complications. 

CASE E: Acute MI

Link to the case:

https://bhavaniv.blogspot.com/2021/05/case-discussion-on-myocardial-infarction.html?m=1

Question 1:
What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

Evolution of symptomatology :
11/5/2021 – Chest pain started
14/5/2021 – Giddiness and profuse sweating (since morning)
 
Anatomical localization – Heart
 
Primary etiology – Patient has a history of Hypertension and Diabetes mellitus which, along with age related plaque formation could be the cause of his current condition.

 
Question 2:
What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
 

	MOA	INDICATIONS	EFFICACY
Tab. Aspirin	CoX inhibitor – reduces PG formation	Angina
Tab. Atorvas	HMG-CoA reductase	Dyslipidemia and risk of DM
Tab. Clopibb	Antiplatelet action	Prophylactic to prevent clot further clot formation
Inj. HAI	Fast acting insulin	High levels of glucose in blood

 

Question 3:
Did the secondary PTCA do any good to the patient or was it unnecessary?

This procedure was followed by placement of stent, which hints at a severe condition and possibility of a future risk of another similar attack. So yes, PTCA was useful in the above case.

CASE F: Cardiogenic Shock 

Link to the case:

https://kattekolasathwik.blogspot.com/2021/05/a-case-of-cardiogenic-shock.html

Question 1:
How did the patient get  relieved from his shortness of breath after i.v fluids administration by rural medical practitioner?

Pathology :

                                                               Congestive Heart failure

↓

Blood backs up in the veins

↓

Pulmonary Bp increases

↓

Fluid pushed into air spaces

↓

Reduced O2 exchange

↓

Shortness of breath

Role of IV fluids

Hypertonic IV fluid introduced into body

↓

Fluids move out of ECF and into the vessels

↓

Reduced pressure on alveoli

↓

Improved O2 exchange

↓

Reduction in SOB

 

Question 2:
What is the rationale of using torsemide in this patient?

• It is a diuretic.
• High creatinine levels suggest improper functioning of kidneys – which might be a result of  heart failure (cardiorenal syndrome) – thus the reduced urine output.
• The diuretic is suggested to get rid of this excessive fluid in the body and reduce pressure on the heart.

 
Question 3:
Was the rationale for administration of ceftriaxone? Was it prophylactic or for the treatment of UTI?

Ceftriaxone – Used as a prophylactic in this case to prevent UTI.

GASTROENTEROLOGY:

CASE A: Pancreatitis with pseudocyst 

Link to the case:

https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-pancreatitis-with.html

Question 1:

What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

Evolution of symptomatology:

5 years ago - Episode of fever and vomiting

6/5/2021 - Pain abdomen and vomiting (since this day)

9/5/2021 - Constipation

                 burning micturition

                 fever

Anatomical localization: Abdomen

Primary etiology: Excessive alcohol consumption

Question 2:

What is the efficacy of drugs used along with other non pharmacological  treatment modalities and how would  you approach this patient as a treating physician?

	MOA	INDICATIONS	EFFICACY
Inj.Meropinam	Broad spectrum antibiotic	Prophylaxis (complications of acute pancreatitis)
Inj.Metrogyl	Antibiotic	Prophylaxis as above
Inj. Amikacin	Antibiotic	Prophylaxis as above
IV NS/RL	Fluid/Electrolyte replacement	Dehydration
Inj. Octreotide	Somatostatin analogue	Excessive pancreatic secretion
Inj.Pantop	PPI	Reduce pancreatic secretions
Inj.Thiamine	Vitamin B1 supplement	Encephalopathy prophylactic
Inj. Tramadol	Analgesic	Pain

CASE B: Acute Pancreatitis: 

Link to the case:

https://nehae-logs.blogspot.com/2021/05/case-discussion-on-25-year-old-male.html

Question 1:

What is causing the patient's dyspnea? How is it related to pancreatitis?

• The cause of dyspnea in this pateint is probably Pancreatitis.
• A severe casse of pancreatitis usualy resukts in Multiorgan failure - most importantly pulmonary complications, the pathogenesis of which is attributed to the production of noxious cytokines.

Pulmonary complications of PANCREATITIS are divided into three stages.

• Stage 1-pulmonary manifestations without any radiological changes
• Stage 2-Showing radiologic changes
• Stage 3-ARDS.

Going by the reports (high levels of amylase and protein) and the above classification our patient falls in the 2^nd stage as we have found PLEURAL EFFUSION on doing chest x-ray.

Question 2:

Name possible reasons why the patient has developed a state of hyperglycemia.

Some pointers/risk factors are:

• Age of patient- due to possible insulin resistance
• Chronic alcohol consumption- initial dip followed by rise dur to prefered digestion of alcohol to glucose.
• Affected Pancreas in the patient- source of insulin damaged leading to Hyperglycemia

Question 3:

What is the reason for his elevated LFTs? Is there a specific marker for Alcoholic Fatty Liver disease?

• Raised LFT values in patient of acute pancreatitis suggests a inflammation of gall bladder caused by gall-stone . 
• ALT and AST r nonspecific indicators of liver disease. The AST > ALT in case of alcoholic Fatty Liver Disease (in contrast to Non Alcoholic case).

Question 4:

What is the line of treatment in this patient?

•  IVF: 125 mL/hr - to maintain body fluid levels and prevent dehydration
•  Inj PAN - as PPI 
•  Inj ZOFER - to control infalmatory damage
•  Inj Tramadol - As analgesic
•  Tab Dolo - Analgesic
•  GRBS charting 6th hourly 
•  BP charting 8th hourly

CASE C: Liver Abscess 

Link to the case:

https://chennabhavana.blogspot.com/2021/05/general-medicine-case-discussion-1.html

Question 1:

What is the most probable diagnosis in this patient?

According to the reports given, the rise in AST and ALT suggest a Liver Abscess.

Other differentials not possible because:

• Organised intraperitoneal hematoma - no history of trauma of any sort
• Right kidney RPD - there is no history/ complaint of back pain
• Subdiaphragmatic fluid collection - radiological evidence deny this possibility.

Question 2:

What was the cause of her death?

Possible cause of death in this case is 

• Decreased Diastolic BP - due to septic shock
• Right lobe atelectasis 

Question 3:

Does her NSAID abuse have  something to do with her condition? How?

Normally, The efferent arterioles of an organ are seen to be constricted.

But with NSAID abuse, even the afferent vessels are constricted leading to increased blood pressure levels .

...

NEPHROLOGY:

CASE A: Post TURP with non oliguric ATN 

Link to the case:

https://kavyasamudrala.blogspot.com/2021/05/medicine-case-discussion-this-is-online.html

Question 1:

What could be the reason for his SOB ?

Acute tubular necrosis

↓

Fluid retention in lungs

↓

O2 exchange effected 

↓

Shortness of breath

Question 2:

Why does he have intermittent episodes of  drowsiness ?

• According to the patient reports(RFT) , there is rise in Urea and creatinine - caused due to kidney injury
• This rise makes tthe pateint drowsy.

Question 3:

Why did he complaint of fleshy mass like passage in his urine?

NOTE : 

• The pateint has a hostory of transurethral resection of prostate(TURP).
• Clot/scab retention is the most common complication of TURP.

Electrocautery during TURP (to reduce bleedimg)

↓

May form clot/scab

↓

Scab passed from urethra after surgery 

↓

perceived as mass passed during urination

Question 4:

What are the complications of TURP that he may have had?

Major complications:

• Clot retension
• Failure to void
• UTI
• Chronic hematuria
• Uncontrolled acute hematuria

Minor complications:

• Sepsis
• Bladder perforation
• Disseminated intravascular coagulation

CASE B: Frequent urination  

Link to the case:

https://drsaranyaroshni.blogspot.com/2021/05/an-eight-year-old-with-frequent.html

Question 1:

Why is the child excessively hyperactive without much of social etiquettes ?

The patient's history points towards a possibility of ADHD - Attention deficit hyperactivity disorder.

Characteristic/suggestive features being : 

• Hyperactive nature
• No social ettiquttes
• No attention at school

Question 2:

 Why doesn't the child have the excessive urge of urination at night time ?

The frequent urge for urination may be either due to 

• Organ damage - which doesnt seem to be the case here
• Psychosomatic origin - stress , anxiety, etc

 Since this patient has a psychosomatic origin for urination, he doesnt show nocturnal enuresis.

Question 3:

How would you want to manage the patient to relieve him of his symptoms?

The following management is suggested:

• Furthur investigation to rule out organic causes - including CBP and USG
• Diagnosis of Anxiety and psychiatric conditions if any.

• In absence of organic cause - treatment should include behavioural therapy
• Ditropan - to reduce frequncy
• ASSURANCE to mother and child.

INFECTIOUS DISEASES:

CASE A: Patient with fever, dysphagia and cough  

Link to the case:

https://vyshnavikonakalla.blogspot.com/2021/05/a-40-year-old-lady-with-dysphagia-fever.html

Question 1:

Which clinical history and physical findings are characteristic of tracheo esophageal fistula?

Positive findings of tracheo-esophageal fistula in above case are:

• History of difficulty in swallowing
• History of cough on food intake
• History of retroviral disease

Associated physical findings are:

• Laryngeal crepitus
• Endoscopy showing proliferative growth in mid esophagus
• Fistulous communication between - left main bronchus and mid thorasic esophagus
• Barium swallow showing abnormal contrast

Question 2:

What are the chances of this patient developing immune reconstitution inflammatory syndrome? Can we prevent it? 

• Chances are high

• Risk factors include:

1. Fever since 2 months
2. Lymph node enlargement in mediastinum
3. TB diagnosis after ART
4. CRP +

INFECTIOUS DISEASE AND HEPATOLOGY:

CASE A: Liver abscess  

Link to the case:

https://kavyasamudrala.blogspot.com/2021/05/liver-abscess.html

Question 1:

Do you think drinking locally made alcohol caused liver abscess in this patient due to predisposing factors present in it ? What could be the cause in this patient ?

Yes, i do believe that locally made alcohol caused Liver Abscess in this patient.

The predisposing factors are :

• Diabetes.
• Liver cirrhosis.
• Immunocompromised state.
• Male sex.
• Advanced age.
• Proton-pump inhibitor use

The causative factor in this case must have been : Chronic alcoholism

Question 2:

What is the etiopathogenesis  of liver abscess in a chronic alcoholic patient ? ( since 30 years - 1 bottle per day)?

Etiology :

• Origin may be : pyogenic ; ameobic ; hydatid cyst; 
• They are mostly acquired from blood stream 

Pathology:

• Most common : Bowel content leakage OR peritonitis - Where bacteria travel via portal vessels.
• In this case bacteria in locally prepared alcohol played a major role.  

Factors involved in association between alcohol and abscess:   

• poor nutritional status - due to alcohol consumption
• Presence of infective organisms in locally made alcohol
• Immunity of patient
• Liver damage

Question 3:

Is liver abscess more common in right lobe ?

Yes, single lesions of liver abscess are more common in right lobe.

The reason being , comparatively more blood supply the lobe receives from superior mesentric vein.

   

Question 4:   

What are the indications for ultrasound guided aspiration of liver abscess ?       

Some indications include:

• Abscess is large - more than 5cm  - chances of rupture Are high.
• Location is left lobe - more chances of peritoneal leak
• Not responding to drugs for more than 7 days

CASE B: Liver abscess  

Link to the case:

https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-liver-abcess.html

Question 1:

Cause of liver abcess in this patient ?

Etiology:

• Pyogenic liver abscess – polymicrobial 

1. Staphylococcus 
2. E .coli
3. Klebsiella
4. Streptococcus

• Amoebic liver abscess – most commonly caused by Entamoeba hisolytica 

In this patient, occasional toddy consumption acted as source of pathogens.

Question 2:

How do you approach this patient ?

Treatment of liver abscess  includes : 

• Empirical antibiotics : cover both bacterial and amoebic causes -

1. For bacterial cause : penicillin +cephalosporin is given ( zostum 1.5 gm i.v. BD injection) 
2. For amoebic cause : metronidazole ( Metrogyl 500mg i.v. TID injection )

• Percutaneous drainage of abscess is not done in this patient because of the response to antibiotic therapy and associated complications of drainage 

• Ultracet to relieve pain 

• Dolo 650 mg for fever 

Question 3:

Why do we treat here ; both amoebic and pyogenic liver abcess? 

Based on the following : 

• Age of patient – 21 yr ( young age ) , male gender 
• Single abscess 
• Right lobe involvement 
• Chest x ray showing no involvement 

              The abscess is more likely to be amoebic liver abscess

              Since we cannot take risk we treated patient for both bacterial and amoebic cause.

Question 4:

Is there a way to confirmthe definitive diagnosis in this patient?

Yes we can confirm the diagnosis in this patient by : 

• Detection of serum antibodies against Entamoeba 
• Culture and sensitivity report of the aspirate

INFECTIOUS DISEASES:

CASE A: Altered sensorium - mucormycosis case  

Link to the case:

http://manikaraovinay.blogspot.com/2021/05/50male-came-in-altered-sensorium.html

Question 1:

What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

Evolution of symptomatology : 

18 -04-2021 - Fever with chills and rigors          
28-04-2021 - Facial puffiness                               
28-04-2021 - Periorbital oedema                         
28-04-2021 - Generalised weakness.  ( Right upper & lower limb )               
4-05-2021 - Altered sensorium                               
4-05-2021 - Serous discharge from left eye        
4-05-2021 - Oral and nasal cavity involvement    

 Anatomical localisation:

Eye 

Nasal & sinus mucosa 

Oral cavity 

Brain 

  Primary etiology :  Rhizopus : fungus 

Question – 2 : 

What is the efficacy of drugs used along with other non pharmacological  treatment modalities and how would  you approach this patient as a treating physician?

Drugs that can be used to treat mucormcosis are : 

1) Amphotericin – B 

• Liposomal 

• Deoxycholate    

2) Posaconazole   

Efficacy of drugs :  

• Liposomal AmpB > Deoxycholate AmpB > Posaconazole 
• Deoxycholate AmpB is cheaper compared to Liposomal AmpB 

Approach to patient : 

• Stabilise the patient 
• Treat the diabetic ketoacidosis 
• Treatment with antifungal preferably Liposomal AmpB 

Question – 3 :

What are the postulated reasons for a sudden apparent rise in the incidence of mucormycosis in India at this point of time?        

  

The reason for recent increase in the cases of mucormycosis is immunocompromised state following recovery from COVID -19 infection

INFECTIOUS DISEASE (Covid-19):

The link to my Master sheet has been provided below:

https://docs.google.com/spreadsheets/d/1iFSWQpYt_44iCpwOLDPIju2MxrQ3Y23JihV_srhW3E0/edit?usp=sharing

MEDICAL EDUCATION:

Experiential learning is a very important method of Medical education and while the E logs of the students in the questions above represent partly their and their patient's experiences, reflective logging  of one's own experiences is a vital tool toward competency development in medical education and research. A sample answer to this last assignment around sharing your experience log of the month can be seen in the link below but while this is by a student onsite in hospital  and not locked down at home we would be very interested to learn about your telemedical learning experiences from our hospital as well as community  patients over the last month even while locked down at home:

 https://onedrive.live.com/view.aspx?resid=4EF578BAE67BA469!4180&ithint=file%2cdocx&authkey=!AOy7BpRTn42DBMo

Answer:

With the subject of General Medicine being one which is clinical in nature, staying locked down at home, far away from the clinical set up and still learning with equal clarity seemed like a huge task until I came across this particular project.

It helped me clear my concepts and gain a better grip over my subject.

I would like to thank Dr. Rakesh Biswas sir for giving me this opportunity to learn beyond the textbook lines and all the Professors, PGs and interns who guided me in doing so.